scholarly journals Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death 4

RSC Advances ◽  
2018 ◽  
Vol 8 (16) ◽  
pp. 8455-8468 ◽  
Author(s):  
Pengwei Lu ◽  
Xue Yang Xue Yang ◽  
Yunqing Yang ◽  
Fang Wang ◽  
Lin Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Programmed Cell Death 4 ◽  
Cancer Tissues

Linc00472 expression was down-regulated in breast cancer tissues and cells, and was associated with the development and prognosis of breast cancer.

scholarly journals Retraction: Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death 4

RSC Advances ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 5895-5895
Author(s):  
Laura Fisher
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Programmed Cell Death 4

Retraction of ‘Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death 4’ by Pengwei Lu et al., RSC Adv., 2018, 8, 8455–8468, DOI: 10.1039/C8RA00296G

LncRNA NEAT1 accelerates breast cancer progression through regulating miR-410-3p/ CCND1 axis

2020 ◽  
Vol 29 (2) ◽  
pp. 277-290
Author(s):  
Xuan Liu ◽  
Weirong Yao ◽  
Haiwei Xiong ◽  
Qiang Li ◽  
Yingliang Li
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Breast Cancer Progression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Cancer Tissues

BACKGROUND: Breast cancer is the most common malignant tumor and usually occurs in women. Studies have shown that lncRNA nuclear enriched abundant transcript 1 (NEAT1) contributes to breast cancer progression. This study intends to further investigate the molecular mechanism of NEAT1 in breast cancer. METHODS: The expression levels of NEAT1, miR-410-3p and Cyclin D1 (CCND1) were detected by quantitative real-time PCR (qRT-PCR) in breast cancer tissues and cells. Kaplan-Meier analysis and the log-rank test were performed to determine the relationship between NEAT1 and overall survival. Cell Counting Kit-8 (CCK-8) assay analyzed cell proliferation. Transwell assay was performed to examine cell migration and invasion. The protein levels of CCND1 and epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin, N-cadherin and Vimentin) were measured by western blot. The target relationship was predicted by bioinformatics analysis, and confirmed by luciferase reporter assay and RNA Immunoprecipitation (RIP) assay. Xenograft analysis was used to evaluate the tumor growth in vivo. RESULTS: NEAT1 and CCND1 were upregulated, while miR-410-3p was down-regulated in breast cancer tissues and cells. Higher NEAT1 expression level was associated with lower survival rate of breast cancer patients. Knockdown of miR-410-3p restored silenced NEAT1-mediated the inhibition of on proliferation, migration, invasion and EMT of breast cancer cells. In addition, NEAT1 regulated CCND1 expression by sponging miR-410-3p in breast cancer cells. NEAT1 knockdown blocked the tumor growth in vivo. CONCLUSION: NEAT1 induced breast cancer progression by regulating the miR-410-3p/CCND1 axis, indicating that NEAT1 may be a potential therapeutic target in breast cancer.

scholarly journals PCAT-1 Facilitates Breast Cancer Progression via Enhancing Oxygen-independent Stability of Hypoxia-inducible Factor-1α

2020 ◽  
Author(s):  
Jianlong Wang ◽  
Xuyi Chen ◽  
Ning Zhang ◽  
Jianzhao Gao ◽  
Bin Liu
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Metabolic Regulation ◽  
Hypoxia Inducible Factor ◽  
Breast Cancer Progression ◽  
Physical Interaction ◽  
Breast Cancer Patients ◽  
Loss Of Function ◽  
Hypoxia Inducible Factor 1Α ◽  
Cancer Tissues

Abstract Background: Hypoxia induces a series of cellular adaptive responses that enable to promote inflammation and cancer development. However, only few have been fully characterized about the roles of long noncoding RNAs (lncRNAs) in hypoxia-associated cancer progression. Methods: The involvement of lncRNAs in hypoxia-related cancer progression was screened by qRT-PCR. Based on the public databases and integrating bioinformatics analysis, the alteration of prostate cancer associated transcript-1 (PCAT-1) in breast cancer tissues was detected and validated in a cohort of breast cancer tissues. Overexpression and knocking down experiments were performed to uncover the biological roles of PCAT-1 on cell hypoxia-associated phenotypes and biological behaviors. RNA immunoprecipitation (RIP) and RNA pull-down were carried out to reveal the physical interaction between PCAT-1 and receptor of activated protein-C kinase-1 (RACK1). Moreover, xenograft mouse models were used to evaluate the influence of PCAT-1 on cancer progression and metastasis in vivo.Results: We identified PCAT-1 as a hypoxia-inducible lncRNA that regulated the hypoxia-inducible factor-1α (HIF-1α) stability, crucial for cancer progression. Extensive analyses of clinical data indicated that PCAT-1 was elevated in breast cancer patients and was associated with pathological grade, tumor size and poor clinical outcomes. Through gain and loss of function experiments, we found that PCAT-1 promoted hypoxia-associated breast cancer progression including growth, migration, invasion, colony formation, and metabolic regulation. Mechanistically, PCAT-1 directly interacted with RACK1 protein and prevented RACK1 from binding to HIF-1α, thus protecting HIF-1α from RACK1-induced oxygen-independent degradation.Conclusions: These findings provide a new insight into lncRNA-mediated mechanisms for HIF-1α stability and suggest that a novel role of PCAT-1 as a potential therapeutic target for breast cancer.

scholarly journals Silencing of KIF3B Suppresses Breast Cancer Progression by Regulating EMT and Wnt/β-Catenin Signaling

2021 ◽  
Vol 10 ◽  
Author(s):  
Chengqin Wang ◽  
Runze Zhang ◽  
Xiao Wang ◽  
Yan Zheng ◽  
Huiqing Jia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Breast Cancer Progression ◽  
Migration And Invasion ◽  
Breast Cancer Cell Lines ◽  
Mesenchymal Transition ◽  
Cancer Tissues

Breast cancer is the most common malignant tumors in women. Kinesin family member 3B (KIF3B) is a critical regulator in mitotic progression. The objective of this study was to explore the expression, regulation, and mechanism of KIF3B in 103 cases of breast cancer tissues, 35 metastatic lymph nodes and breast cancer cell lines, including MDA-MB-231, MDA-MB-453, T47D, and MCF-7. The results showed that KIF3B expression was up-regulated in breast cancer tissues and cell lines, and the expression level was correlated with tumor recurrence and lymph node metastasis, while knockdown of KIF3B suppressed cell proliferation, migration, and invasion both in vivo and in vitro. In addition, UALCAN analysis showed that KIF3B expression in breast cancer is increased, and the high expression of KIF3B in breast cancer is associated with poor prognosis. Furthermore, we found that silencing of KIF3B decreased the expression of Dvl2, phospho-GSK-3β, total and nucleus β-catenin, then subsequent down-regulation of Wnt/β-catenin signaling target genes such as CyclinD1, C-myc, MMP-2, MMP-7 and MMP-9 in breast cancer cells. In addition, KIF3B depletion inhibited epithelial mesenchymal transition (EMT) in breast cancer cells. Taken together, our results revealed that KIF3B is up-regulated in breast cancer which is potentially involved in breast cancer progression and metastasis. Silencing KIF3B might suppress the Wnt/β-catenin signaling pathway and EMT in breast cancer cells.

scholarly journals Forkhead box P3 promotes breast cancer cell apoptosis by regulating programmed cell death 4 expression

2020 ◽  
Vol 20 (6) ◽  
pp. 1-1
Author(s):  
Dong Fan ◽  
Cheng Zeng ◽  
Shuming Wang ◽  
Jun Han ◽  
Liaoliao Zhu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Apoptosis ◽  
Forkhead Box P3 ◽  
Cancer Cell Apoptosis ◽  
Forkhead Box ◽  
Programmed Cell Death 4

scholarly journals Long non-coding RNA ROR recruits histone transmethylase MLL1 to up-regulate TIMP3 expression and promote breast cancer progression

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Aixia Hu ◽  
Fan Hong ◽  
Daohong Li ◽  
Yuwei Jin ◽  
Lingfei Kon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Cancer Prognosis ◽  
Non Coding Rna ◽  
Novel Target ◽  
Cancer Tissues ◽  
Long Non Coding Rna

Abstract Background As a significant cause of cancer deaths worldwide, breast cancer continues to be a troublesome malignancy. Long non-coding RNAs (lncRNAs) have been implicated in the development of breast cancer. Abnormal methylation has been associated with unfavorable breast cancer prognosis. Herein, the current study aimed to elucidate the role of lncRNA ROR in breast cancer. Methods RT-qPCR was performed to determine whether lncRNA ROR was highly expressed in breast cancer tissues, while lncRNA ROR expression was detected in both the nuclear and cytoplasm of breast cancer cells. MCF-7 cells were subsequently introduced with oe-lncRNA ROR, sh-lncRNA ROR to explore the effects of lncRNA ROR on cell proliferation, invasion and apoptosis. Results RIP, RNA pull-down and ChIP assays provided evidence suggesting that lncRNA ROR recruited transmethylase MLL1 to promote H3K4 trimethylation that enhanced TIMP3 transcription. The rescue experiments demonstrated that lncRNA ROR knockdown could inhibit the progression of breast cancer via the downregulation of TIMP3. Finally, the in vivo experiment findings consistently highlighted the suppressive effects of lncRNA ROR silencing on tumor growth. Conclusion Taken together, our study demonstrates that silencing of lncRNA ROR inhibits breast cancer progression via repression of transmethylase MLL1 and TIMP3, emphasizing the potential of lncRNA ROR as a novel target against breast cancer.

scholarly journals Circular RNA circCCDC85A inhibits breast cancer progression via acting as a miR-550a-5p sponge to enhance MOB1A expression

2022 ◽  
Vol 24 (1) ◽  
Author(s):  
Lingjiao Meng ◽  
Sheng Chang ◽  
Yang Sang ◽  
Pingan Ding ◽  
Liuxin Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Breast Cancer Progression ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Qrt Pcr ◽  
Cancer Tissues

Abstract Background A growing body of evidence indicates that abnormal expression of circular RNAs (circRNAs) plays a crucial role by acting as molecular sponges of microRNAs (miRNAs) in various diseases, including cancer. In this study, we explored whether circCCDC85A could function as a miR-550a-5p sponge and influence breast cancer progression. Methods We detected the expression of circCCDC85A in breast cancer tissues and cells using fluorescence in situ hybridization (FISH) and quantitative reverse transcription polymerase chain reaction (qRT-PCR). CCK-8 and colony formation assay were used to detect the proliferative ability of breast cancer cells. Wound healing assay and transwell migration and invasion assays were used to detect the migrative and invasive abilities of breast cancer cells. We also examined the interactions between circCCDC85A and miR-550a-5p using FISH, RNA-binding protein immunoprecipitation (RIP), and luciferase reporter assay. Moreover, we performed luciferase reporter assay, qRT-PCR, and Western blot to confirm the direct targeting of miR-550a-5p to MOB1A. Results The expression of circCCDC85A in breast cancer tissues was obviously lower than that in normal breast tissues. Over-expression of circCCDC85A substantially inhibited the proliferative, migrative, and invasive ability of breast cancer cells, while knocking down of circCCDC85A enhanced the aforementioned properties of breast cancer cells. Moreover, enforced expression of circCCDC85A inhibits the oncogenic activity of miR-550a-5p and increases the expression of MOB1A targeted by miR-550a-5p. Further molecular mechanism research showed that circCCDC85A may act as a molecular sponge for miR-550a-5p, thus restoring miR-550a-5p-mediated targeting repression of tumor suppressor MOB1A in breast cancer cells. Conclusion Our findings provide novel evidence that circCCDC85A inhibits the progression of breast cancer by functioning as a molecular sponge of miR-550a-5p to enhance MOB1A expression.

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